ArticleProceedings of the National Academy of Sciences of the United States of America2003
CTCF functions as a critical regulator of cell-cycle arrest and death after ligation of the B cell receptor on immature B cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 72 citations in OpenAlex.
- Deciphering resistance mechanisms to auxin-inducible protein degradation in mammalian cells.The Journal of biological chemistry · 2026Article
- ACLY integrates metabolism and chromatin accessibility to enable B Cell activation and humoral immunity.bioRxiv : the preprint server for biology · 2026Article
- Deciphering acquired resistance mechanisms to sustained auxin-inducible protein degradation in cells and mice.bioRxiv : the preprint server for biology · 2025Article
- CTCF is selectively required for maintaining chromatin accessibility and gene expression in human erythropoiesis.Genome biology · 2025Article
- DNA architectural protein CTCF facilitates subset-specific chromatin interactions to limit the formation of memory CD8Immunity · 2023Article
- Association of mutation and low expression of theSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020Article
- Article
- Acute depletion of CTCF directly affects MYC regulation through loss of enhancer-promoter looping.Nucleic acids research · 2019Article
- CCCTC-binding factor is essential to the maintenance and quiescence of hematopoietic stem cells in mice.Experimental & molecular medicine · 2017Article
- Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia.Cancer research · 2017Article
- Rare variants at 16p11.2 are associated with common variable immunodeficiency.The Journal of allergy and clinical immunology · 2015Article
- Early targets of miR-34a in neuroblastoma.Molecular & cellular proteomics : MCP · 2014Article
- CCCTC-binding factor mediates effects of glucose on beta cell survival.Cell proliferation · 2014Article
- NF-kappa B mediated up-regulation of CCCTC-binding factor in pediatric acute lymphoblastic leukemia.Molecular cancer · 2014Article
- Ribosomal RNA gene transcription mediated by the master genome regulator protein CCCTC-binding factor (CTCF) is negatively regulated by the condensin complex.The Journal of biological chemistry · 2013Article
- Epidermal growth factor (EGF)-induced corneal epithelial wound healing through nuclear factor κB subtype-regulated CCCTC binding factor (CTCF) activation.The Journal of biological chemistry · 2013Article
- BORIS, brother of the regulator of imprinted sites, is aberrantly expressed in hepatocellular carcinoma.Genetic testing and molecular biomarkers · 2013Article
- Genome-wide studies of CCCTC-binding factor (CTCF) and cohesin provide insight into chromatin structure and regulation.The Journal of biological chemistry · 2012Review
- Overexpression of the human ZNF300 gene enhances growth and metastasis of cancer cells through activating NF-kB pathway.Journal of cellular and molecular medicine · 2012Article
- CTCF mediates effect of insulin on glucagon expression.Experimental cell research · 2012Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The WEHI 231 B cell lymphoma is used as a model of self-tolerance by clonal deletion because B cell receptor (BCR) ligation results in apoptosis. Two critical events precede cell death: an early rise and fall in expression of MYC and cell-cycle arrest associated with enhanced expression of p21, p27, and p53. CTCF is a transcription factor identified as a repressor of MYC recently shown to cause cell growth inhibition. The present studies demonstrate that BCR ligation of WEHI 231 as well as of normal immature B cells greatly increased expression of CTCF in association with down-regulation of MYC followed by growth arrest and cell death. Conditional expression of CTCF in WEHI 231 mimicked BCR ligation with activated cells showing repressed expression of MYC, enhanced expression of p27, p21, p53, and p19(ARF), and inhibition of cell growth and induction of apoptosis. In keeping with a central role for CTCF in control of B cell death, conditional expression of a CTCF antisense construct in WEHI 231 resulted in inhibition of p27, p21, p53, and p19(ARF) in association with enhanced expression of MYC. Activation of the endogenous CTCF locus by BCR ligation was also mimicked by three other routes to apoptotic death in WEHI 231: inhibition of the phosphoinositide 3-kinase or mTORFRAP signaling cascades and treatment with transforming growth factor (TGF)-beta. Rapid activation of CTCF by BCR ligation or treatment with TGF-beta was suppressed by ligation of CD40. These results demonstrate that CTCF is a common determinant to different pathways of death signaling in immature B cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.